Simona Frateschi
Lausanne, VD 1011, Switzerland
Last Updated: 09/26/2026
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Found 9 publications
Kidney-Specific CAP1/Prss8-Deficient Mice Maintain ENaC-Mediated Sodium Balance through an Aldosterone Independent Pathway.
Journal: International journal of molecular sciences
Published: May 18, 2022
Lack of Renal Tubular Glucocorticoid Receptor Decreases the Thiazide-Sensitive Na+/Cl- Cotransporter NCC and Transiently Affects Sodium Handling.
Journal: Frontiers in physiology
Published: March 18, 2019
The function and regulation of acid-sensing ion channels (ASICs) and the epithelial Na(+) channel (ENaC): IUPHAR Review 19.
Journal: British journal of pharmacology
Published: January 28, 2016
Adult nephron-specific MR-deficient mice develop a severe renal PHA-1 phenotype.
Journal: Pflugers Archiv : European journal of physiology
Published: November 20, 2015
Severe Salt-Losing Syndrome and Hyperkalemia Induced by Adult Nephron-Specific Knockout of the Epithelial Sodium Channel α-Subunit.
Journal: Journal of the American Society of Nephrology : JASN
Published: February 11, 2015
Regulation of blood pressure and renal function by NCC and ENaC: lessons from genetically engineered mice.
Journal: Current opinion in pharmacology
Published: November 25, 2014
The channel-activating protease CAP1/Prss8 is required for placental labyrinth maturation.
Journal: PloS one
Published: April 27, 2012
Mutations of the serine protease CAP1/Prss8 lead to reduced embryonic viability, skin defects, and decreased ENaC activity.
Journal: The American journal of pathology
Published: December 22, 2011
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Last Updated: 09/26/2026